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Pathophysiology - Endocrine and Reproductive > Pharmacology of Diabetes Mellitus > Flashcards

Pharmacology of Diabetes Mellitus Flashcards

1
Q

What are the hypotheses which link adiposity to insulin resistance?

A
  1. Toxicity of circulating fats
  2. Endocrine effects of adipose tissue -> release of leptin, resistin, and TNFa / IL-6 which control inflammation
  3. Inflammation from ectopic fat storage -> in liver and visceral organs, causes insulin resistance
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2
Q

What are the three sulfonylureas primarily being used today?

A
  1. Glimepiride
  2. Glipizide
  3. Glyburide

Think of the two ducks “riding” mother goose, and a smaller goose making a “z” in the ice for glipiZide

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3
Q

What are the adverse reactions of sulfonylureas?

A
  1. Induction of severe hypoglycemia
  2. Stimulation of appetite (due to hypoglycemia) -> weight gain
  3. High failure rate as disease progresses (beta cell failure)
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4
Q

What are the meglitinides? What is their claim to fame?

A

Repaglinide
Nateglinide

“Nate be Rapping cuz he so fly”

  • > non-sulfa drug sulfonylureas, but more short-acting.
  • > think of the goose “gliding” / flying in the air
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5
Q

What is the current first line treatment for diabetes and what is its mechanism of action?

A

A biguanide called metformin

Lowers blood glucose levels without stimulating insulin release.

  1. Reduces gluconeogenesis (reduced liver output)
  2. Enhances insulin action on peripheral tissues (reduces resistance)

Modifies mitochondrial enzymes to do this

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6
Q

What are the adverse effects of metformin use and who is it contraindicated in?

A

GI disturbances -> dose-related, especially at start of therapy -> girl about to puke

Lactic acidosis (from decreased usage of lactate in gluconeogenesis)

-> avoid in renal insufficiency (Decreased clearance of metformin, not metabolized hepatically)

Spilled milk in broken kidney tray

Also avoid in liver disease, or alcoholics

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7
Q

What are the thiazolidinediones (TZDs) also called? What drugs are in this class?

A

Glitazones - think of glitter

Includes:

  1. Rosiglitazone - roses are red
  2. Pioglitazone
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8
Q

What is the mechanism of action of the TZDs and what drug are they similar to?

A

Similar to metformin, in that they reduce insulin resistance without posing hypoglycemia risk

Mechanism:

  1. Activate PPARy (Remember this guy’s shirt is the life of the party (PPARy), don’t get confused with PPARa of the fibrates) receptor, expressed in white adipocytes which is a nuclear transcription factor. This upregulates ADIPONECTIN! (Think adiponectin turtle neck).
  2. Also think of the open candy mailbox nearby -> also increases insulin sensitivity.
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9
Q

What are the adverse effects of glitazones? How does this relate to their usage

A

This keeps them from being used alot, only used as second line in combination:

  1. Congestive heart failure from 2. Edema -> baggy pants and heart failure baloon
  2. Weight gain -> significant, due to induced differentiation of hepatocytes (guy holding donuts)
  3. Bone loss -> broken chair leg banging into heart failure balloon
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10
Q

What drug is a human GLP-1 with a mutation making it DPP-4 resistant? What is the other drug in this class?

A

Liraglutide
Other drug: Exantide
-these are the ones that end in tide.

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11
Q

What are the actions of exenatide and liraglutide? Benefits? Main side effect of concern?

A

Induces insulin release, depresses glucagon release, and delays gastric emptying (like amylin + insulin release) -> good for post-prandial surge

  • > associated with significant weight loss!
  • > liraglutide even approved for obesity
  • > probably due to feeling of satiety from delayed gastric emptying

Side effect: Think of the -Tide cleaning witch holding the sponge (acute pancreatitis)

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12
Q

What drug is a DPP-4 inhibitor, and what is its primary benefit over the GLP-1 homologs? What is its main side effect?

A

Sitagliptin (Januvia)
- think of the gliptin clips (4 clips for DPP-4)

Can be taken orally, does not show GI disturbances.

However, no associated weight loss :/

Side effect: upper respiratory tract infections (think of the clothespin on the lady’s nose)

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13
Q

What is SGLT2 vs SGLT1?

A

Both combine to reabsorb all glucose if blood level is <200 mg/dL

SGLT2 - high capacity, low affinity transporter in kidney, co-transports sodium and glucose

SGLT1 - low capacity, high affinity, prevents hypoglycemia by taking up glucose from urine when your body REALLY needs it

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14
Q

What are the SGLT2 inhibitors?

A

Dapagliflozin
Empagliflozin
Canagliflozin

end in -gliflozin
-> think flozin floss

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15
Q

What are the clinical uses / benefits of SGLT2 inhibitors?

A

Taken orally, modest HbA1c reduction in combination with metformin.

Also reduces CVD outcomes and may promote weight loss due to excretion of glucose

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16
Q

What are the risks of SGLT2 inhibitors?

A
  1. Urinary tract yeast infections -> due to glucose in urine. Think of the Canada flag and kid throwing snowball.
  2. Diabetic ketoacidosis (rare, perhaps from hypoglycemia)
  3. Dehydration - from diuresis

Avoid in renal insufficiency

17
Q

Do DPP4 inhibitors and GLP-1 produce hypoglycemia? How about meglitinides or sulfonylureas? Metformin?

A

DPP4 / GLP-1: No

Meglitinides (lower risk) / Sulfonylureas: Yes

Metformin: No

18
Q

What drug is an amylin analog again? How does it work? What types of diabetes can it be used in?

A

Pramlintide (think lynn) -

Amylin - think of empty glucose packets (suppressed glucagon) and the decreased gastric emptying (gastric water cooler)

Can be used in both Type 1 and Type 2 diabetes, think of the girls holding up one and two fingers.

Think of Amy and Lynn, the twins he asked to be his valentine. Damn you braden!

19
Q

When is Pramlintide used and what are its side effects?

A

Think of the spilled candies and braden getting sick to his stomach

GI upset and hypoglycemia

-> used for cupcakes (around mealtime, control of postprandial glucose surge)

20
Q

What are the alpha-glucosidase inhibitors and how do they work?

A

Acarbose and miglitol (wiglitol gummy bears)

Inhibit disaccharidase-mediated monosaccharide formation at brush border
-> obviously cause diarrhea and shit

21
Q 
Tell me if the following classes of drugs have demonstrable cardiovascular benefits or harms?
Metformin:
GLP1: 
SGLT2:
DPP4:
TZDs:
A 
Metformin: Definite benefit
GLP1: Definite benefit (weight loss)
SGLT2: Benefit
DPP4 (gliptins): Neutral (possible increase in HF exacerbations)
TZDs (glitazones): Harm (heart failure)
22
Q

At what threshold should Type 2 diabetes begin dual therapy and then insulin treatment?

A

Dual therapy: 9%

Insulin: HbA1c >10%

23
Q

What drug monitoring is required for the TZDs and what should pioglitazone be avoided in?

A

Liver function tests (may be hepatotoxic)

Avoid pioglitazone in patients with a history or FHx of bladder cancer

24
Q

What adjustment should be made empirically before starting GLP-1 agonists i.e. exanatide and liraglutide?

A

Empirically reduce sulfonylurea dose to reduce risk of hypoglycemia

25
Q

What are the possible adverse effects of insulin injections?

A

Hypoglycemia
Lipodystrophy
Weight gain
Rare hypersensitivity reactions (especially if one of the animal derivates of insulin)

26
Q

What are the best sites to inject your insulin?

A

Abdomen > thigh > upper arm

27
Q

If you combine NPH / regular insulin is the insulin concentration profile predictable?

A

No - mixing insulin does not always yield predictable pharmacokinetic parameters

Also, these two types of insulin in particular are very unpredictable

28
Q

What is the general insulin giving scheme for Type 1 and Type 2 diabetics?

A

Give basal, long-acting insulin once daily, and then pre-meal bolus doses of rapid-acting insulin to keep glucose under control.

Add more insulin at meals if fasting plasma glucose is not recovering

Keep in mind GLP-1 analogs can still be used in Type 2

29
Q

What are the rapid, short-acting, intermediate, and long-acting insulins:

A

Girls And Lads, Rest Now, Don’t Go

Glulisine
Aspart
Lispro

Regular - short acting
NPH - intermediate

Detemir
Glargine

30
Q

What type of insulin should be given in DKA and why?

A

Regular insulin -> it’s the only one which can be given IV

Pathophysiology - Endocrine and Reproductive (27 decks)

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